Good morning, and welcome to the Evelo Biosciences Third Quarter 2020 Financial and Operating Results Conference Call. [Operator Instructions]. At this time, I'd like to turn it over to Jessica Cotrone of Evelo. Please proceed..

Thank you, Operator. Good morning, everyone. This morning, we issued a press release that outlines the topics we plan to discuss today. This release is available at www.evelobio.com under the Investors tab.

Today on our call, Simba Gill, Chief Executive Officer; Mark Bodmer, President of R&D and Chief Scientific Officer; and Duncan McHale, Chief Medical Officer; will review our third quarter 2020 financial results and recent business highlights.

Before we begin, I'd like to remind everyone that statements made during this conference call that do not relate to matters of historical facts, including statements about our objectives and anticipated clinical milestones, the impact of any of our product candidates and the timing and results of any clinical studies should be considered forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements are intended to be subject to the safe harbor protection provided by the Reform Act. Actual results could differ materially from those indicated by the forward-looking statements due to the impact of many factors.

Participants are directed to the risk factors set forth in Evelo's quarterly report on Form 10-Q for the quarter ended June 30, 2020, and the company's other filings with the Securities and Exchange Commission. Any forward-looking statements made today speak only to Evelo's operations as of today.

Evelo disclaims any duty to provide updates to its forward-looking statements even if subsequent events cause the company's views to change. It is now my pleasure to pass the call over to Simba..

Thank you, Jessica. Good morning, everyone, and thanks for joining us to review our third quarter and recent progress. 2020 continues to be a transformational year for Evelo, and we have now shown that we can harness SINTAX to resolve inflammation after oral delivery of EDP1815 in humans. These data underpin our development programs.

The Evelo team and our partners have consistently executed on our research and clinical plans, including through the COVID-19 pandemic. And because of this, we are poised to deliver 6 data readouts over the next 3 to 9 months in psoriasis, atopic dermatitis, COVID-19 and triple-negative breast cancer.

These readouts will not only inform our understanding of our current product candidates and programs but also provide important insights about our entire platform, which continues to evolve and expand. Long term, we aim to capture the full breadth and depth of targeting SINTAX across different biologies and diseases.

Mark's team in research and development continue to explore, enhance and expand the applications of SINTAX-based medicines, and he will tell you more about this later on the call.

With an eye to 2021 and beyond, we are making significant progress towards bringing these critical therapies to patients with inflammatory diseases and cancer, who have a need for safe, effective convenient and affordable therapies. And with that, I'll pass the call over to Duncan to discuss our clinical highlights..

Thank you, Simba, and good morning, everyone. I'm pleased to be able today to discuss how we've continued to execute our clinical plans across the entire portfolio over the past quarter. And before updating you on the progress we have made in our clinical programs, I wanted to briefly mention the key opinion leader event we hosted last week with Dr.

Benjamin Ehst, a Board-certified dermatologist and leading clinical investigator. The focus of the event was the current treatment landscape, unmet need and opportunity for EDP1815 in both psoriasis and atopic dermatitis. In his presentation, Dr. Ehst made 3 key points.

Patients with mild to moderate psoriasis and atopic dermatitis have a serious disease with a significant impact on their quality of life.

Dermatologists and patients alike are dissatisfied with existing therapies from the inconvenience and poor adherence of topical treatments through to the expense, risk and need for injections of the biologic agents.

He highlighted the need for a safe, well-tolerated, affordable and efficacious oral treatment, which could be used as monotherapy from mild all the way through to the severe disease as well as in combination with current therapies in the severe disease setting.

Based on the preclinical and clinical research to date, he felt EDP1815 could potentially fit this profile, offering an effective, safe and convenient option to patients, and thus, filling an immense treatment gap. The potential of EDP1815 has also been catching the attention of the dermatology community more generally.

Earlier today, my colleague, Dr. Douglas Maslin, Clinical Lead of Immunology at Evelo, presented data from our Phase Ib clinical trial in mild to moderate psoriasis at the European Academy of Dermatology and Venereology, or EADV, Virtual Congress.

Our poster was selected as one of EADV's key stories and highlighted at a virtual press conference at the event this morning. Now with regard to the clinical programs, as you know, earlier this month, we started our Phase II dose-ranging trial in mild to moderate psoriasis and dosed our first patients.

Just to remind you, the Phase II trial is evaluating 3 doses of EDP1815 versus placebo in approximately 225 patients over a 16-week treatment period.

The primary endpoint is the main reduction in psoriasis area and severity index, or PASI, score, in addition to key secondary endpoints, including the physician's global assessment, lesion severity score and a range of patient-reported outcomes.

This longer dosing period of 16 weeks will give us a better understanding of the potential clinical benefit that EDP1815 could bring to patients with psoriasis.

Interim results from this trial are expected by mid-2021, and the data we generate may enable us to advance into confirmatory registrational studies, following meetings with health authorities in the U.S. and Europe. So now moving to atopic dermatitis.

In October, we completed the enrollment of a cohort of patients with mild to moderate atopic dermatitis in our Phase Ib trial of EDP1815. This cohort is evaluating EDP1815 in enteric capsules versus placebo in 24 patients over a 56-day treatment period.

The primary endpoint is safety and tolerability and will be our first cohort evaluating dosing beyond 28 days. We will also be evaluating a range of secondary endpoints, including markers of atopic dermatitis, like the eczema area and severity index, or EASI, score and the scoring atopic dermatitis, or SCORAD, score.

In addition, we're also collecting a range of patient-reported outcomes, including the Dermatology Life Quality Index and the Pruritus numerical rating score. We expect to report data in the first quarter of 2021.

Atopic dermatitis is the most common chronic inflammatory skin disease and affects an estimated 10% of adults and 25% of children worldwide. It typically presents in a red, intensely itchy rash. And although it's often thought of as a pediatric condition, many will continue to have symptoms throughout their lives.

And as we know from our ongoing psoriasis trial, and as patients and key opinion leaders continue to reinforce, dermatological diseases extend far beyond the individual lesions or flare-ups that can be treated with simple topical treatments. Atopic dermatitis is no different, and as Dr.

Ehst discussed, it is associated with a substantial physical and psychosocial burden on both patients and their families. Thus, as we think about the ongoing development of our product candidate, we are committed to providing a treatment option that improves quality of life as well as improving independent measures of disease. Moving now to COVID-19.

Patients continue to be recruited into our 2 COVID-19 trials, a Phase II trial in partnership with Rutgers University in the U.S. and a Phase II/III trial called TACTIC-E, sponsored by the Cambridge University Hospitals NHS Foundation Trust and led by Addenbrooke's Hospital in Cambridge, U.K.

Now as a result of the varied infection rates that have occurred with the pandemic, we've experienced slower-than-expected enrollment early on in both of the studies, and we now expect to report data from both trials in the second quarter of 2021.

In order to expedite patient recruitment and expand access to potential therapies for COVID-19, new trial sites are being opened for TACTIC-E.

Over the past few months, it has become increasingly clear that COVID-19 will continue to severely impact our global communities, even as tremendous advances are made towards preventing infections and treating the virus.

EDP1815 has the potential to be a truly differentiated treatment for COVID-19 with a Goldilocks-type activity observed preclinically, whereby hyperinflammation is resolved, whilst mechanisms responsible for the antiviral activity are preserved.

When combined with the favorable tolerability of EDP1815 observed in our Phase I trial, it suggests a truly differentiated potential to treat COVID-19, either alone or in combination with other treatments.

And the data from these trials will also provide important learnings as we evaluate future opportunities in viral diseases and other indications involving hyperinflammation. If the data from these trials are positive, we plan to engage in discussions with global regulatory authorities to determine an appropriate path of registration in COVID-19.

So now turning to oncology. As we discussed in our prior earnings calls, we have focused our EDP1503 trial on patients with triple-negative breast cancer. We have continued to recruit into this cohort, and we'll report the new data from our Phase I/II trial at the 2020 San Antonio Breast Cancer Symposium to be held virtually from December 8 to the 11.

With that, I will turn the call over to Mark to discuss our preclinical work..

Thanks, Duncan. As you've heard, we're busy with a wide range of products and development and the clinical results to come. And that's the tip of the iceberg.

As Simba said, we are delving deeper and deeper into the potential of engaging with small intestinal access, SINTAX, to create this extraordinary new class of effective, safe, oral and affordable medicines. A major topic of my remarks today is the new form of SINTAX medicines, bacterial extracellular vesicles, bacterial exosomes, if you like.

This is a hugely exciting new frontier for our platform, which I'll tell you more about shortly. As well as new forms, we are looking at new microbes to learn about the range of therapeutic utility of taxonomically distinct strains, EDP1867 is a good example of this.

We are looking at new formulations, optimizing drug concentration, dispersal and dose, which are critical to getting the most from our products. We are looking at neuroinflammation in preclinical models.

SINTAX can modulate CNS inflammation without needing to get drugs across the blood-brain barrier, solving one of the most pressing problems in CNS drug development. And we're looking at metabolism where we see effects of our agents on visceral fat inflammation and benefits to metabolic profile.

To give you a context for extracellular vesicles, I'm going to take you on a quick tour for 4 breakthroughs that have taken us from our origins as a microbiome company to where we are today. The first breakthrough was based on looking directly at the interactions of microbes with host cells in the gut rather than attempting to fix microbial ecology.

That led us to the efficacy of single strains of microbes and got around the complex challenges of trying to modify the microbiome itself. The second breakthrough was the discovery that the site of action of these single strains was the small intestine, which has a very low microbial content, and not the colon with its trillions of microbes.

We coined the term small intestinal access, or SINTAX. This is more than branding. It's a scientific definition of the control network that radiates throughout the body from the small intestine and that our drugs target and engage.

This turned out to be consistent with the long-standing observation that people who've had a total colectomy have normal immune, neurological and metabolic functions. They have no colon, so they lack those trillions of microbes and live physiologically normal, healthy lifespans. I first got interested in this, actually, some time ago.

A close family member of mine is one of those people with no colon. And it also turned out that the microbes with interesting properties came not from the kilo of stuff that grows in the colon every day but from the rarer microbes that live in the mucosal surfaces that line the gut.

The third breakthrough was realization that our drugs did not need to be alive to be affective. We discovered that the efficacy of our products was still there if the bacteria were not living. This turned out to be a general property of medicines targeting SINTAX and it took us to EDP1867, which is gamma irradiated, like so dead by design.

There are clear benefits to this, in addition to providing formal proof in animals and humans that we are making pharmacological agents rather than microbiome drugs.

And the fourth breakthrough is today's extension of our platform to extracellular vesicles, certain types of bacteria, mostly gram-negative, naturally shed exosomes, generally called extracellular vesicles, or EVs. EVs are lipid vesicles, which contain various elements of the parent bacterium in a volume about 1,000x smaller.

There is a literature on bacterial EVs, including experimental immunomodulation by injection in animal models. There is no literature on systemic immunomodulation by orally delivered bacterial EVs. And yet, that is exactly what we see, dose-dependent effects of pharmaceutical preparations of bacterial EVs from single strains delivered orally.

This discovery gives us a new proprietary nonmicrobial modality of orally delivered SINTAX medicines, which are striking efficacy in preclinical models, both inflammation and oncology. They are working through engagement of the small intestinal access to send signals around the body.

We have not detected distribution of EVs outside the gut preclinically. And they have their effects in mice at doses, which are, by weight, at least 1,000x and up to 100,000x lower than whole microbes. You've seen EDP2939 on our recent pipeline chart as an anti-inflammatory candidate.

This is an EV, which is an advanced preclinical and manufacturing development. In oncology, we recently discovered a bacterial strain which makes EVs with anti-tumor activity in mice that surpasses anything we have previously seen with either a checkpoint inhibitor or a whole microbe, whether in our hands or in the literature.

Indeed, in preclinical tumor models, it is as effective after oral administration as our reported intratumoral immune stimulators. That's a high bar, which this orally dosed EV meets.

Preclinical data on our oncology candidate, called EDP1908, will be presented at the forthcoming meeting of the Society for Immunotherapy of Cancer, SITC, in mid-November in a couple of weeks' time. So we have arrived at the next phase of the Evelo platform, taking our origins in the microbiome to a new level of drug development.

We sometimes joke about our foresight of having EV at the start of the company name, Evelo. Of course, there was no foresight, but we've had the good fortune that came from keeping open to ever-greater possibilities of the extraordinary potential of the drugs that act on SINTAX. Now back to Simba..

Thank you, Mark. As I mentioned at the beginning of the call, we have 6 clinical readouts expected over the next 3 to 9 months.

Within our COVID-19 programs, we expect initial data from a Phase II trial in partnership with Rutgers University as well as interim safety data and futility analysis from the Phase II/III TACTIC-E trial in the second quarter of 2021.

We also expect data from our Phase Ib trial of EDP1815 and EDP1867 in atopic dermatitis in the first quarter of 2021 and mid-2021, respectively, and interim data from our Phase II trial in mild to moderate psoriasis by mid-2021.

Finally, we will report additional data from our Phase I/II clinical trial of EDP1503 in triple-negative breast cancer at the San Antonio Breast Cancer Conference in December.

In addition, as Mark mentioned, we look forward to sharing initial preclinical data for EDP1908, our first extracellular vesicle candidate for oncology, at the SITC meeting in a couple of weeks. This is an incredibly exciting time for Evelo.

We have now entered Phase II clinical development of EDP1815 and our advancing a pipeline of potential medicines which could transform the care of millions of patients living with inflammatory disease and cancer worldwide.

Alongside our clinical development effort, we continue to optimize our candidates through rigorous preclinical evaluation and testing and look forward to capitalizing on our growing knowledge to expand our platform.

Our developments with microbial extracellular vesicles expand our ability to harness SINTAX, and we're excited to advance our EV programs into development.

We are progressing with significant momentum and moving closer and closer to delivering a broadly applicable new class and profile of medicine that is not only efficacious but also safe and well-tolerated, orally delivered and affordable.

We have accomplished a lot over the last quarter, and this would not have been possible without the passion and commitment of our team, who I'd like to thank. And with that, I'll now open the call for questions..

[Operator Instructions]. Our first question comes from the line of Chris Howerton with Jefferies..

Can you hear me now?.

Yes, sir, we can hear you..

Okay. Sorry about that. Anyway, I was just saying, congratulations on the quarter and the progress. And obviously, some exciting times coming forward. So I guess, just a couple of questions for me.

One would be, what is your -- I think there's been some kind of tantalizing increases in terms of neuro inflammation and the applicability of that science for CNS disorders. So I'd be curious to know what your application for 1815 might be in those types of medical indications.

Secondly, if you can give us a little more color or granularity on what we might expect at San Antonio Breast Cancer by the end of this year in triple-negative breast cancer. As you all know, I've followed the Immunomedics story for quite some time, so obviously, Trodelvy has made a lot of noise in that space.

So just curious to see what we will learn from your 1503 program and what the updates might be specifically at that conference.

And then lastly, with respect to the extracellular vesicles, I guess, what is the drug product that you're envisioning? And I'm sorry if I missed it, and what is the purity of the drug substance or the content themselves of the extracellular vesicles? And I think maybe I'll stop there..

Okay. Chris, thank very much. Let me answer your question about the cancer conference, the San Antonio Cancer Conference in December. And then I'm going to pass over to Mark, who, I think, can, first of all, answer the EV question, can give you the scientific background behind what we're doing in neuro inflammation and why we're excited about it.

And if we need more clarity on the clinical and neuro, Duncan can give you our initial thoughts there. So on the San Antonio Breast Cancer Conference, what we've basically said is that we will report data there on roughly 20 patients who are in the existing combination study with KEYTRUDA.

To your point on Trodelvy, we see that level of response as well as other relevant data from patients as essentially the bar, Chris. So if we see something in the order of 25% to 30% response rate, then we have something that could be very interesting to take forward. And so we'll be reporting out on that in 20 patients.

Importantly, it's not competitive with Trodelvy. As you know, Chris, it's something that's complementary. The way we look at the current world of IO is there's essentially three pillars, obviously, checkpoints. Many of them now have removed the break that is applied to the immune system by tumor cells.

Things like Trodelvy and the several approaches there increase exposure to antigen -- neoantigen in a tumor microenvironment.

And what we're able to do based on a preclinical and early clinical data with EDP1503 and our next wave of programs in oncology is to activate the innate and, subsequently, the adaptive immune systems with something that is orally delivered and something that appears to be very safe and well tolerated.

So it's a very nice fit with other things that are going on in the IO world. So that's what we'll be reporting out on. And as I said, if we see something similar to Trodelvy in terms of response rate, that's something very interesting and would, in principle, support potentially going to later-stage clinical trials.

Obviously, if we see something at a lower level, then it potentially is still interesting in terms of supporting activation of systemic immunity, consistent with what I've just described. So that's what we're waiting for there.

Let me pass over to Mark, who can talk about -- maybe I'll just address, Mark, the EV response first, and then you can respond on neuro inflam. And if there's anything, you don't get to, Duncan can talk about your neuroinflammation..

Sure. Chris, Mark here. So the drug product is a natural component of the fermentation. Actually, it's the part we normally throw away because the extracellular vesicles are shed from the bacteria into the medium. And so rather than harvesting the cells, we harvest the medium.

And we purify it by a mixture of centrifugation and filtration, it's fairly straightforward. I'm going to answer your questions about purity and content in a regulatory context because I suspect that's part of what you have in mind in asking it. And we have discussed these questions with regulatory authorities, both in the U.S.

and in the U.K., with very positive outcomes because they recognize that the extracellular vesicles were part of or likely to be part of the types of products that we are already using in the clinic as whole microbe.

So actually, the preclinical development requirements we have for EVs at the moment don't look to be any different from the microbes, which is hugely beneficial because as you'll recall, we haven't had to do preclinical toxicology testing.

And because these are natural products, orally delivered, the requirements for purity are completely different than they would be, for instance, if we were making a mammalian exosome and trying to inject it intravenously or by some other parenteral route. So there's a permissive path for these things that are -- that's the same as for the microbes.

One other comment about the drug product itself. If we look at dose yield per liter of fermentation, which is where essentially the cost and scale issue will come, it's pretty similar for the EVs as it is to the whole microbes. It actually may even be a little bit higher. So we haven't changed our manufacturing scale requirements.

It just changes the downstream processing a bit. And then content, so the EVs basically grab parts of the macro molecular content of the parent bacterium. It's not a one-for-one matching, and we're doing a lot of our own mix at the moment to try and look at that.

But of course, we've got to hairball of data showing that some proteins are more highly represented in the EV versus the bacterium and the other way around. And we're looking at glycolipids and the rest.

And the differences we're seeing in the efficacy, which you'll see in the SITC conference shortly between the whole microbe and the EV maybe due to differences in content. I suspect it's much -- it's more to do with the pharmacodynamics of the EV and its ability to get to the target. So that's where we are with that.

I hope that answers your question there..

Yes.

And I'm sorry, Mark, but maybe just a very brief clarification in it's basically -- it's a lyophilized product in a capsule? Is that the dosage form?.

Yes, sorry. Yes, it's a lyophilized product. It takes the lyophilization in the same way that microbes do. We're looking at all the same formulation questions with the EVs that we are with the microbes and actually transferring the technology straight over.

There are differences in disbursements and lyophilization excipients and things, but it's fundamentally the same process..

Okay. All right. Well, very exciting..

The briefing on the -- yes, it's very exciting, actually. It's extraordinary if you think back to where I think 4 years ago that we're able to reduce it for something like this. So it's really transformational, and we'll talk more about some of the scientific details behind this in the coming months as well. It's really -- it's a new world.

On the neuro inflammation, the key point there is actually the one I made a moment ago on the formal part of the call that the activity of the microbes in the small intestine bypasses the need to cross the blood-brain barrier because SINTAX, the small intestinal access, does it for us.

And we have put a lot of these data in the public domain or some of it is published by our collaborators at the Mayo Clinic. We can clear inflammatory cells in the central nervous system -- actually, you can take spinal cord sections, you see it very clearly. And that's a profound statement.

Actually, that statement alone would be enough to base an entire company on with the prospects for doing something. And there are companies that are actually based on fundamental ideas about how you can get pharmacological activity in the central nervous system, and that's what we do.

It hasn't been part of our mainstream development yet, but it has been a significant part of what we've been doing preclinically. You asked the question specifically in the context of EDP1815. Actually, the preclinical models are ones where we've seen some differentiation in the robustness and maximum efficacy of different microbes.

And so we have 2 other microbes, which actually have superior pharmacology in the preclinical models, the EDP1815. EDP1815 works, part of it is basic on inflammatory activity, but these others give us more consistent and robust activity. We'll talk about that more as things develop.

So interestingly, as we go in -- out from core inflammation to neuro inflammation, and actually, I mentioned metabolism as we look in some of the inflammatory aspects of metabolic control, we're starting to see some degree of differentiation amongst our product candidates that we didn't see just looking at core classical inflammatory models.

And so I'll leave it there I think..

Our next question comes from the line of Joseph Thome with Cowen & Company..

The first one is on the atopic dermatitis programs.

When we see data from 1815 and 1867 next year, can you just remind us how you're thinking about moving forward in the indication? If both look good, would you move both forward? Or would you make a decision before kind of further committing in the indication? And then with the data from the COVID-19 studies, if this looks effective here, do you believe there's a role for 1815 in other pulmonary viral conditions? And will this be an area of focus outside of COVID if the data looks strong?.

Thanks, Joe.

So on the first question, our strategy has always been to look at different microbes which are differentiated in terms of, for example, in the inflammatory space, how they're driving inflammation resolution and are different in other ways, linked to manufacturing, linked to behavior in the small intestine and the gut, and that's why we're taking 1815 and 1867 forward.

So they're different, but they're both very potent in resolving inflammation in preclinical models. The way we sometimes refer to it is it's like looking at antibodies, which are both targeting the same diseases but work on different mechanisms and different pathways.

And then the answer to your question is it's going to be devil in the details, and let's see what the data is. Obviously, if 1815 drives potent responses in atopic dermatitis, we're going to move it forward aggressively, and we'll still continue to see what happens with 1867. So we have to see the data, Joe.

But at the moment, we've got somewhat of an embarrassment of riches in having 2 very potent anti-inflammatory agents that work on different mechanisms. So we'll see what the data reveals there.

On 1815, if we see a response in COVID, as your question suggests, it's got very broad utility in a number of other viral infections, pulmonary and beyond, because the core driver of the theory as to why we're looking at 1815 in COVID, as you know, Joe, is to resolve the hyperinflammation that causes progression to serious COVID-19.

And that same principle of hyperinflammation is relevant to a number of other viral infections, including influenza, for example, which is still killing significant numbers of people in the world, as you know, and in a number of other areas. So yes, absolutely, we'll look into other areas if we see positive results in COVID-19..

And our next question comes from the line of Matthew Luchini with BMO Capital Markets..

This is Jen [ph] on for Matthew. Congrats on the progress. Just two questions for me.

Could you guys provide some color on what you guys are doing in terms of the trial sites expansion? Like just how many sites are being added? And when they're coming along -- coming online? And does that mean there's going to be a change in geographic makeup of the study in some way?.

Jen, good to hear your voice. So let me step back a little bit, and then I'll answer your question directly, Jen. So obviously, the world of COVID-19 is complex and unpredictable. What we've been doing to essentially set ourselves up for rapid and accelerated recruitment is exploring opening up new sites not just in the U.K.

but absolutely in other geographies. And we have multiple discussions ongoing right now. As you know, this is part of a U.K. platform study led by Addenbrooke's. We're working very closely with them, but it's their study. So I don't think it's appropriate for me to say more right now other than we are looking to expand sites not just in the U.K.

but also internationally in some of the obvious areas where COVID-19 continues to be significant. And I expect we'll be able to say more in the not-too-distant future, Jen ..

Got it.

And my other question is could you remind us how the Phase II psoriasis trial helped accelerate development in AD?.

Yes, sure.

Duncan, do you want to take that one?.

Sure. Thanks, Jen [ph] for the question. Obviously, there's a lot of learnings that we will be able to take from the EDP1815 psoriasis program for atopic dermatitis. I think, in short, all of the safety tolerability data is very likely to just extrapolate completely across these very similar populations from that perspective.

Also from the dose response data combined with our Phase Ib cohort that's currently ongoing will provide an awful lot of information actually about the dose as well. So we'll be able to take both safety, tolerability and, in fact, the efficacy learnings from psoriasis and apply those to the atopic dermatitis program..

[Operator Instructions]. I'm not showing any further questions. I'll now turn the call back over for closing remarks..

Thanks very much, everyone, for continued attention to what we're doing. As you heard on today's call, this is an incredibly exciting time, both in terms of the clinical readouts we're moving forward as well as progress in terms of advancing the platform with our extracellular vesicles as well as progress in other areas of disease and biology.

So appreciate the continued attention to Evelo, and we look forward to keeping you updated as we go forward. Thank you very much..

Ladies and gentlemen, this does conclude the program. You may now disconnect. Thank you for participating. Everyone, have a great day..